title: Impaired visual evoked flow velocity response in cerebral amyloid angiopathy.
abstract: OBJECTIVE
  Animal models of cerebral amyloid angiopathy (CAA) exhibit abnormal vascular reactivity. We determined whether vascular reactivity, measured by transcranial Doppler ultrasound (TCD), is reduced in humans with CAA.
  
  
  METHODS
  Cases were recruited from an established prospective study of CAA. Healthy controls were recruited from a study of normal aging. Evoked mean flow velocity increase in the posterior cerebral artery (PCA) was measured while subjects viewed a flashing alternating checkerboard stimulus. In a separate but partially overlapping cohort we measured the mean flow velocity increase in the middle cerebral artery (MCA) while subjects inhaled carbon dioxide.
  
  
  RESULTS
  The visual evoked mean flow velocity increase was 8.0 +/- 6.1% in CAA (n = 11) compared to 17.4 +/- 5.7% in controls (n = 9, p = 0.002). The PCA pulsatility index, a marker of distal vascular resistance, was higher in CAA (CAA 1.35 +/- 0.35, control 1.04 +/- 0.14, p = 0.03). Among CAA subjects, lower visual evoked mean flow velocity increase was associated with a higher number of hemorrhages seen on MRI (r = -0.87, p = 0.0005) and higher MRI white matter hyperintensity volume (r = -0.67, p = 0.02). The MCA response to carbon dioxide did not differ between CAA and control in 20 subjects (9 CAA, 11 control, p = 0.54).
  
  
  CONCLUSIONS
  Cerebral amyloid angiopathy (CAA) was associated with decreased vascular reactivity in response to visual stimulation, possibly reflecting the occipital predilection of the disease. The association of posterior cerebral artery (PCA) evoked flow velocity response with elevated PCA pulsatility index and MRI markers of small vessel disease suggests that abnormal PCA evoked flow velocity in CAA is caused by pathology of the distal resistance vessels.
authors.affiliation: Harvard Medical School, 175 Cambridge Street, Suite 300, Massachusetts General Hospital, Boston, MA 02114, USA. eesmith@partners.org
authors.forename: E E
authors.initials: EE
authors.lastname: Smith
authors.forename: M
authors.initials: M
authors.lastname: Vijayappa
authors.forename: F
authors.initials: F
authors.lastname: Lima
authors.forename: P
authors.initials: P
authors.lastname: Delgado
authors.forename: L
authors.initials: L
authors.lastname: Wendell
authors.forename: J
authors.initials: J
authors.lastname: Rosand
authors.forename: S M
authors.initials: SM
authors.lastname: Greenberg
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001783:Blood Flow Velocity / Q000502:physiology; D016657:Cerebral Amyloid Angiopathy / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D006801:Humans; D008137:Longitudinal Studies; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D020769:Posterior Cerebral Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D012044:Regression Analysis; D012189:Retrospective Studies; D014057:Tomography, X-Ray Computed / Q000379:methods; D017585:Ultrasonography, Doppler, Transcranial / Q000379:methods